Polycystic ovary syndrome (PCOS) is one of the most common endocrinopathies that affects 5-7% of reproductive age women world-wide [1]. It is associated with hyperandrogenemia/hyperandrogenism, anovulation, infertility, and a characteristic ovarian morphology consisting of multiple small subcortical follicular “cysts” embedded in bilaterally enlarged ovaries [2-5]. The presence of an elevated level of circulating testosterone results primarily from increased production of androgens by the ovaries, and is a classical endocrine phenotype of women with PCOS. Although there has been debate about the diagnostic criteria for PCOS, hyperandrogenemia/hyperandrogenism and anovulation, not explained by other causes, is a hallmark of the disorder, and is included as a key element in all “consensus” diagnosis schemes [6-10]. There is consensus that the ovarian theca cells are the primary source of excess androgen biosynthesis in women with PCOS [11-13]. Studies on freshly isolated theca tissue, or cultures of theca cells derived from normal and PCOS women have demonstrated that PCOS theca secretes greater amounts of androgen than theca tissue or cells from regularly ovulating women [12, 14-19]. Increased thecal androgen biosynthesis in PCOS theca cells results from increased expression of the key enzymes involved in androgen biosynthesis, cytochrome P450 17 alpha hydroxylase (encoded by the CYP17A1 gene) and cytochrome P450 cholesterol side chain cleavage (encoded by the CYP11A1 gene) [15-17, 20].